The molecular basis by which RNA tumor viruses cause disease has been studied and two methods have to date been elucidated: (1) the replicating type-C virus, by being deleted and then recombining with either cell or other viral information, forms a rapidly transforming replication-defective virus This virus is associated with sarcomas and leukemias characterized by a short incubation period. The virus is deleted specifically in information for envelope gp70 and core protein polymerase, and sometimes more or less of the gag structural protein: (2) a second method, a model for leukemias of long incubation caused only by nontransforming replicating viruses, is suggested by experiments demonstrating that, if morphologically flat mink cells nonproductively infected by MSV are superinfected by replicating leukemia type viruses, they become transformed concomitant with an increase in sarcoma virus RNA. This would indicate that certain leukemias in animals may occur by increasing, during replication of usually nontransforming leukemia viruses, the levels of RNA from potentially oncogenic but normal cell genes or integrated viral transforming genes. BIBLIOGRAPHIC REFERENCES: Peebles, P. T., Gerwin, B. I. and Scolnick, E. M.: Murine sarcoma virus defectiveness: Serological detection of only helper virus reverse transcriptase in sarcoma virus rescued from nonmurine S+L- cells. Virology 70: 313-323, 1976. Peebles, P.T., Scolnick, E. M. and Howk, R. S.: Increased sarcoma virus RNA in cells transformed by leukemia viruses: Model for leukemogenesis. Science, 192: 1143-1145, 1976.